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-  2017 

Environmental toxin acrolein alters levels of endogenous lipids, including TRP agonists: A potential mechanism for headache driven by TRPA1 activation

DOI: 10.1016/j.ynpai.2017.03.001

Keywords: 2-AG, 2-arachidonyl glycerol, AA, arachidonic acid, AEA, N-arachidonoyl ethanolamine, A-GABA, N-arachidonoyl GABA, A-Phe, N-arachidonoyl phenylalanine, A-Ser, N-arachidonoyl serine, A-Taur, N-arachidonoyl taurine, A-Tyr, N-arachidonoyl tyrosine, CER, cerebellum, CNS, central nervous system, d8NAGly, deuterium labeled N-arachidonoyl glycine, DAG, diacylglycerol, DEA, N-docosahexaenoyl ethanolamine, D-Gly, N-docosahexaenoyl glycine, DMEM, Dulbecco’s Modified Eagle’s Medium, eCB, endogenous cannabinoid, FAAH, fatty acid amide hydrolase, FBS, fetal bovine serum, HPLC/MS/MS, high pressure liquid chromatography coupled to tandem mass spectrometry, KO, knockout, LEA, N-linoleoyl ethanolamine, L-Gly, N-linoleoyl glycine, MAGL, monoacylglycerol lipase, NAE, N-acyl ethanolamine, NAGly, N-arachidonoyl glycine, OEA, N-oleoyl ethanolamine, O-Gly, N-oleoyl glycine, O-Phe, N-oleoyl phenylalanine, O-Val, N-oleoyl valine, PEA, N-palmitoyl ethanolamine, PG, prostaglandin, PLC, phospholipase C, P-Phe, N-palmitoyl phenylalanine, S-Gly, N-stearoyl glycine, S-Phe, N-stearoyl phenylalanine, TG, trigeminal ganglia, TNC, trigeminal nucleus caudalis, TRP, transient receptor potential, TRPA1, TRP ankyrin 1, TRPV1, TRP vanilloid 1, TVS, trigeminovascular system Lipidomics, Endogenous cannabinoid, TRPA1, TRPV1, Lipoamine, Acrolein, Migraine

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Abstract:

Exposure to airborne toxins can trigger headaches, but the mechanisms are not well understood. Some environmental toxins, such as acrolein, activate transient receptor potential ankyrin 1 (TRPA1), a receptor involved in pain sensation that is highly expressed in the trigeminovascular system. It has been shown in rat models that repeated exposure to acrolein induces trigeminovascular sensitization to both TRPA1 and TRP vanilloid 1 (TRPV1) agonists, a phenomenon linked to headache. In this study, we test the hypothesis that the sensitization of trigeminovascular responses in rats after acrolein exposure via inhalation is associated with changes in levels of endogenous lipids, including TRPV1 agonists, in the trigeminal ganglia, trigeminal nucleus, and cerebellum. Lipidomics analysis of 80 lipids was performed on each tissue after acute acrolein, chronic acrolein, or room air control. Both acute and chronic acrolein exposure drove widespread alterations in lipid levels. After chronic acrolein exposure, levels of all 6 N-acyl ethanolamines in the screening library, including the endogenous cannabinoid and TRPV1 agonist, N-arachidonoyl ethanolamine, were elevated in trigeminal tissue and in the cerebellum. This increase in TRPV1 ligands by acrolein exposure may indicate further downstream signaling, in that we also show here that a combination of these TRPV1 endogenous agonists increases the potency of the individual ligands in TRPV1-HEK cells. In addition to these TRPV1 agonists, 3 TRPV3 antagonists, 4 TRPV4 agonists, and 25 orphan lipids were up and down regulated after acrolein exposure. These data support the hypothesis that lipid signaling may represent a mechanism by which repeated exposure to the TRPA1 agonist and environmental toxin, acrolein, drives trigeminovascular sensitization

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